The over production of acid in the gut of an animal by microorganisms can cause fermentative acidosis, wherein is defined as a condition of abnormally high acidity in the gut that can lead to local and systemic acidosis, damage to the integrity of the gut wall and increased pathogenicity of gut bacteria and parasites.
The introduction of starch, sugars or oligosaccharides into the rumen of ruminant animals and the hind gut (caecum and colon) of ruminant and non-ruminant animals including humans, leads to rapid fermentation and production of volatile fatty acids (VFA). As the rate of VFA production exceeds their rate of removal, the pH may fall below 6.0, such that lactobilli take over, fermenting the starch to produce more lactic acid and creating an even lower pH (e.g. below 5.5). This is the scenario often presented to describe the sequential reactions in the rumen or the hind gut that lead to fermentative acidosis. The conditions of acidosis can be acute, posing an immediate life-threatening situation, or chronic (sub-acute), resulting in reduction in both feed intake and weight gain. There are also numerous disease conditions that can develop as secondary and tertiary consequences of acid accumulation in the gut.
Among the several methods for reducing the risk of acidosis, the use of antibiotic feed additives such as virginiamycin or certain ionophores have been relatively effective. However, under certain feeding conditions addition of virginiamycin has not always reduced the risk of acidosis (Godfrey et al., 1995; Courtney and Seirer, 1996; Thomiley et al., 1998).
Accordingly, there is a need to provide alternative means of controlling fermentative acidosis.
The main bacterial species and strains identified in the present invention, Clostridium-like species, Prevotella-like species, Bacteroides-like species, Enterococcus-like species, Selenomonas species, non-dextran slime producing Streptococcus species and non-slime producing lactic acid bacterial isolates, have not previously been considered to be important organisms in the development of fermentative acidosis. In fact, in the case of Selenomonas ruminantium it should be noted that the isolate selected by Leedle (1970) was identified on the basis of its ability to utilise lactic acid, rather than produce it and is therefore very different to the isolates that form part of the present invention.
Therefore, the present invention has identified a series of microorganisms responsible for the development of acidosis and describes vaccines, compositions and methods for the treatment and/or prevention and/or detection of acidosis in vertebrates.